Spontaneous, asynchronous, myocardial calcium oscillations, have been attributed to calcium-dependent calcium release form the sarcoplasmic reticulum (SR) and exhibit a periodicity which depends upon the extent of cell calcium loading. In thin excised cardiac muscle the inhomogeneous contractile motion caused by the spontaneous oscillations phase modulates a laser beam passed through thin excised cardiac muscle, producing intensely fluctuations in the scattered light (SLIF). In the present project we measured intensity fluctuations of 633 nm laser light backscattered from the epicardial surface of isolated, perfused rat and rabbit hearts. The frequency of SLIF was increased by maneuvers that raise intracellular calcium. SLIF were abolished by removal of extracellular calcium with ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid and by blockade of SR calcium release by ryanodine. SLIF were not accompanied by any surface electrocardiogram and were not abolished by 144 mM extracellular potassium. SLIF were absent in rabbit hearts under base-line conditions but could be provoked by calcium loading using zero potassium and ouabain. Thus, SLIF monitors the microscopic motion caused by intracellular calcium oscillations in the intact heart. Delayed recovery of contractile function after myocardial ischemia may be due to increased calcium loading. To examine this potential mechanism, SLIF were studied in isolated atrioventricularly blocked rat hearts during and after 60 min of ischemia at 30 degrees C. After reperfusion developed pressure evidenced a small recovery but then fell abruptly. This was accompanied by an increase in end-diastolic pressure to 37+/-5 mm Hg and a fourfold increase in SLIF, to 252+/-58% of baseline. In another series of hearts initial reperfusion with calcium of 0.08 mM prevented the SLIF rise and resulted in improved developed pressure (74+/-3% of control), and lower cell calcium (5.9+/-3 vs 10.3+/-1.4 micromol/g dry wt). Thus, during reperfusion delayed contractile recovery can be attributed, in part, to an adverse effect of calcium loading which can be indexed by increased SLIF occurring at that time.